Veterinary science / 1. Veterinary medicine

Types of the animal thyroid gland diseases

Master of veterinary sciences Raketsky V.A.

Kostanay state university of A.Baytursynov, Kazakhstan

Fundamentally, every thyroid gland autoimmune disease is due to the antigen-specific defect in the function of suppressor (regulatory) cell. In the thyroid gland autoimmune disease the suppressor cells are activated worse by an appropriate antigen, but they preserve the ability for the normal activation by the other antigen, normally suppressor cells’ reaction to both antigens is indistinguishable. The presented disorder, as such, isn’t enough for the autoimmune disease induction. In this case, there is a necessity in the additional adverse influences of the outside environment on the immune system. Such influences reduce the total activity of the regulatory cells, and this reduction has an impact on the genetic-associated dysfunction of the specific T-suppressors [1].

Another extrinsic factor, affecting the natural development of the immunologic thyroiditis is iodine intake. Much evidence points to the adverse influence of the iodine on the thyroid gland function and the antibody level in humans with an apparent and hidden autoimmune thyroid gland disease. As for the sensitive people, iodine may provoke an acute development of the hypothyroid [2]. At least two mechanisms may account for the effect of iodine, they are Tg immunogenicity and inhibition of the iodine conversion into organic. Thyroiditis - inflammatory diseases that occur in the intact thyroid gland. The development of inflammation in the goiter modified thyroid gland is called strumitis. Etiology and pathogenesis of these diseases are not fully discovered; typically the cause of thyroiditis is an acute and confirmed infection with a different primary site. In the first place there are various inflammations of nasopharyngeal region (sore throat, influenza, carious teeth, etc.)[3].

Acute thyroiditis refers to a rare thyroid gland disorder. The reason of its emergence is acute and long-lasting inflammatory diseases beyond the thyroid gland (tonsillitis, pneumonia, osteomyelitis, erysipelatous inflammation, furunculosis, scarlet fever, staphylomycosis and streptococcemia and other). Infection goes to the thyroid gland with blood or lymphoma from the inflammatory areas. Diffuse toxic goiter (DTG) (Basedow's disease, Graves' disease) is found everywhere. The disease is due to the hyper-incretion thyroid thyroxin and triiodothyronine, and primarily characterized by changes in the cardiovascular and nervous system. Primary iodine deficit in the diffuse toxic goiter is not diagnosed, the ethiology of the disease is not defined. The disease provokes acute and confirmed infections (influenza, tonsillitis, rheumatism, acute and long-lasting tonsillitis, tuberculosis and other), hypothalamic-pituitary axis disease, pregnancy, iodine intake in large dozes [4].

Recent researches have demonstrated that patients with thyrotropine diffuse toxic goiter have normal or even lower consentration in the pituitary body and blood. It’s suggested that the main role in the disease process play: the long-acting thyroid stimulator, occurring in the thymus gland and lymphocytes, the violation in the immunologic process, and also the sensibility elevation of the adrenergic receptors to catecholamines [5].

In the development of the thyrotoxicosis clinical findings the great importance is either attached to the sympathetic nervous impulses, coming in the theroid glang through its sympathetic nervous. It is believed that the sympathetic nervous impulses of the thyroid gland increase the thyroid hormone appearance and production. The preponderance of the more active triiodothyronine hormone is true to form over the less active tetraiodiothyronine hormone [5].

There is, apparently, an important role in the disease process, also belonging to the tissular diiodase. The enhancement of the latter promotes the thyroid hormone tissure action. There is a strong probability that a certain role in the disease process belongs to the thyroid hormone dysmetabolism in the peripheral tissues - liver, kidneys and muscles. This results in a formation and rather quick decomposition of such active metabolites as the triiodothyroacetic acid, etc.

The inhibition of the conversion from carbohydrate into fat, as well as the inhibition of the hyposensitive sympatic nerve terminals in the fatty tissue to the adrenaline action happen under the influence of the thyroid hormone excessive production. This leads, together with low glycogen content in the liver, to the increased fat mobilization from its storage and the patient’s loss weight. The thyroid hormone excess leads to a water-salt metabolism disorder; this is evidenced by the increase of water displacement, sodium chloride, calcium, phosphorus and kalium to a lesser extent, the content of the linked magnesium increases in blood serum [3].

According to M.I. Balabonkin, P.S. Vetshev, E.A. Valdina [3,4,5] the goitre pathology is marked by three morthological forms: diffuse, junctional and mixed. Microscopically, these forms are characterized by significant heterogeneity. Thyroid gland pathology caused by toxic goiter is defined by the follicular gland polymorphism, its lumina mutation, hypertrophy and hyperplasia of the follicular epithelium cells, assuming a spool-shaped form and constituting the papillomatous proliferation in the follicular gland lumina. Dispersoid is liquid, low eosinophilic. Blood vessels are congested. Lymphocyte aggregates with a lymphatic follicle build-up are found in the connective tissue. In some cases the hyperplasia is noticed in the thymus gland, amygdaloid bodies and lymph glands.

It is, sometimes, diagnosed the adrenal hypoplasia case with a reduction in cortex to the complete atrophy of the latter. In a number of instances, ‘thyrotoxic encephalopathy’ is discovered and often accompanied by the dystrophic changes of nerve cells in the tween-brain and olivary nuclei. The main consequence of the iodine deficiency in the environment is the development of goiter among people living in iodine deficiency regions (endemic goiter). In this regard, it has long been assumed that goiter is the only manifestation of this state. It is proved that, in addition to goiter, the iodine deficiency has other negative effects on human health and animals. Insufficient iodine intake in the body results the hypothyroidism, reflecting a slowing of the metabolism and, primarily, oxidation processes; the basal metabolism increase and body temperature [6]. In 1983, the term ‘endemic goiter’ was replaced by ‘Iodine Deficiency Disorder’ (IDD). These diseases are caused by the decrease of the thyroid gland functional activity in response to iodine deficiency. The defect in the iodine diets is the main cause of goiter among animals, which leads to the reduction of oxidation processes and nitrogen metabolism, and also enhances the adipopexia. Iodine deficiency in adult animals is marked by a failure in the sexual cycles, miscarriages, underdeveloped and puffy newborns. In some cases, even a dead animal yield is born [3]. Hypothyroidism may arise as a result of the goitrogenic agent actions, which cause a violation of the thyroid hormone synthesis and correspondingly increased production of TSH, leading to the thyroid compensatory hypertrophy that depends on the goitrogen dose and iodine level, entering the body. It is known that iodine is a necessary component of the thyroid hormone synthesis. So, thyroxine (T4) 65% and triiodothyronine (T3) 59% consist of iodine. Consequently, the deficit of iodine is accompanied by decrease of the thyroid hormone level, i.e. the decrease of the thyroid gland functional activity.

List of used information resources:

1. Volpe R. Autoimmune diseases of the thyroid gland //Thyroid gland diseases. English translation / Under the editorship of L.I. Braverman. - М.: Medicine, 2000.-P. 140-173.

2. Volpe R. Autoimmune diseases of the endocrine system /R.Volpe //CRC, Boca Raton. 1990. P. 1-364.

3. Valdina E.A. Diseases of the thyroid /Е.А.Valdinf. – 2 ed. SPB.: Petersburg, 2001.-416 p.

4. Hamitova A.M. Hypothyrosis and its preventive care /А.М.Hamitova, А.N.Yunusova. - Kazan, 1979. - 80 p.

5. Balabolkin М.I. Differential diagnostics and treatment of endocrinopathy: Guidebook / M.I.Balabolkin, Е.I.Кlebanova, V.М.Kremneskaya. — М.: Мedicine, 2002. - P. 185 - 344.

6. Аlyoshin B.V. Hypothalamus and thyroid gland /B.V.Alyoshin, V.I.Gubitskiy. - М.: Medicine, 1983. - 184 p.